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. 2017 Dec 8;15:125–134. doi: 10.1016/j.redox.2017.12.002

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© 2017 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 5 — Maf-S inhibition causes a decrease in GSC number by promoting GSC differentiation. (A, B, C and H) GSC number in testes with ND75 or CncC knockdown decreases as compared to that in control testes. (D and H) maf-S knockdown testes also show decreased number of GSCs, suggesting that Maf-S is required for GSC homeostasis. (E, F and H) Inhibitory effects of Maf-S on GSC number in cncC^+/- and in keap1^+/- testes. (G and H) Ectopic expression of Maf-S rescues the inhibitory effects of ND75 on GSC number, suggesting that Maf-S acts as a downstream effector of high ROS-associated GSC differentiation. (A, B, C, D, I) Bam-positive germ cells in testes expressing ND75^RNAi, cncC^RNAi or maf-S^RNAi are detected closer to hub cells as compared to those in control testes. (E, F and I) Inhibitory effects of Maf-S on GSC differentiation in cncC^+/- and in keap1^+/- testes. (G and I) Ectopic expression of Maf-S rescues the ND75^RNAi phenotype of GSC differentiation. Error bar is SEM from more than three independent experiments. Significance was assessed using one-way ANOVA with post-hoc Bonferroni test (*p<0.05, ****p<0.0001). Scale bar, 10 µM. *hub cells.